So let’s go back to some nursing pediatric resuscitation basics here. Epi dose for peds is 0.01 mg per kg. Sure – we all know that (or at least we should). But how do we make the Epi push needed to bridge until we get our Epi drip dialed in for the crashing pediatric patient? You just need to create your own 10cc BristoJet of Epi in a dose that matches your pediatric patient’s weight! Read the article for more detail, but here is the meat and potatoes:

Step 1 – get your pediatric resuscitation Epi push dose (the aforementioned 0.01 mg/kg) and draw it up into a 10cc syringe.

Step 2 – dilute the dose with NS until the 10cc syringe is full.

Step 3 – push 1 cc at a time for your crashing patient- the same as you would for an adult.

This is a really cool article that gets into a great and simple method of making emergent Epinephrine pushes bedside. The folks at R.E.B.E.L.em call this an Epi-Spritzer. (Apparently there are a lot of names circulating for this type of bedside Epi push.) Either way what ends up happening here is a 1mcg/kg push, 1 cc at a time, from a 10cc syringe – and there is evidence that this may be best practice. All of the evidence, of course, is outlined beautifully (with hyperlinks) in the article itself.

Rob Bryant writes for R.E.B.E.L.EMabout theBICAR-ICU study published in Lancetthis past July. The paucity on 8.4% Sodium Bicarbonate (BristoJet 50ml) pushes for critically ill patients is pretty amazing. We all understand the simple concept behind the bicarb push – but do we know the data? This is what FOAMed is all about -taking something we take for granted and putting it to the test of a literature review. Are we using best practice? If not – what can we do better?

BICAR-ICU illustrated some good results in favor of bicarb use with patients at risk for or suffering from AKI. Some interesting advice here for ED folks as well – especially concerning kidney injury patients, the cursory AKIN score, and which boarding ICU patients we may want to suggest, or not suggest, bicarb drips and pushes for. If you need a refresher on the AKIN score and why it is useful for ED/ICU nurses justvisit this page on derangedphisology.com.

Total EM’s podcast #113talks about which patients should get a head CT when they present with minor head trauma and endorse use of blood thinners. The podcast is a response to anew article published by the British Journal of Heamatolgythat shows some surprising numbers – this meta-analysis shows up to 11% of patients presenting to the ED with minor head trauma may have head bleeds if they are on blood thinners.

There are some obvious issues with the paper – there are over 10,000 studies that could have been used, and the authors chose only 4, the exact definition of “minor” head trauma is not easily agreed upon , Warfarin was probably over represented as the thinner most often used within the population, etc etc etc…. But the takeaways here are good and the numbers are similar to other studies that have been broken down on previous FOAMed sites such ashereon R.E.B.E.L.em, andhereon St Emlyn’s. Takeaways here include:

We should probably be advocating for head CT in all patients on blood thinners that have even minor head trauma – even if the GCS is 15

We now have some interesting numbers to back our recommendations if the patient is iffy about heading to CT

Common rule-out scales for head CT might not work on this particular patient population. The Canadian Head CT/Trauma Injury(aka the CCHR – linked here on MDCalc) and the New Orleans Criteria (aka the NOC – linked here on MDCalc)are both not applicable because patients on blood thinners were excluded from the studies verifying the sensitivity and specificity of the rule-out criteria.

Keep these numbers in mind when assigning triage levels to patients with even the most minor head trauma. Even if they present in no distress and an obvious AOx4 and GCS of 15 – it is probably a good idea to up-triage and to the team know what just walked into the waiting room.

First10EM is the site I’ve chosen to dive into the craziness set off by the SPLIT trial and the SMART trial. If you haven’t taken a look at these studies, you might as well click on the links (if you have access). But even if you’ve never heard of either of them, you are probably going to feel the effects if you work in an ED or ICU. I’ve mentioned before that you might start noticing LR replacing some of your typical NS orders. Well, these trials are probably the reason for the switch.

The discussion really hits its stride when it gets toIV fluid choice part 2: The SMART trial.TheSMART trial was published in the NEJMback in March of 2018. Since then it has caused a bit of a stir to say the least. But while most folks tend to think that this trial shows the evils of NS, Justin may be in the minority here by doing a bit of statistical regression. Some issues with the study as outlined within the article by First10EM:

The study has a very high fragility score when placed into a fragility index calculator

The p-value of the primary outcome is 0.04 – while acceptable it is anything but ideal within a discussion of something as important as fluid resuscitation standards

The primary outcome p-value itself is potentially up for discussion (maybe?).

The studies population selection seems strange – a quote from First10EM:

“Only half of these patients were admitted from the emergency department, so extrapolation to ED practice isn’t easy. I will also note that this seems like a very healthy group of ICU patients, with only ⅓ using mechanical ventilation, and only ¼ receiving a vasopressor. That doesn’t sounds like any ICU I have worked in. The amount of fluid used was tiny, and not in keeping with most ICU practice I have seen. I would not have expected to see a difference in outcomes from only a single liter of fluid. Would we have seen bigger differences if larger volumes of fluid were used? Or does the tiny amount of fluid used decrease the biologic plausibility of this finding?”

Either way, even if you are oblivious to the primary literature itself, the SPLIT trial will probably cause a bit of friction in the near future. You’ll be hanging NS and then cancelling it and changing it to LR and back and forth … I can’t wait for shift changes, so the new attending can switch everything up based on their strongly held beliefs for or against the outcomes of this trial.

EMCrit has a wonderful review concerning idiopathic VT.VT is not a single thing – there are multiple different sub-types. Despite what we are typically taught via our every-two-year-AHA-merit badge approach, the knowledge that VT isn’t a single monolithic diagnosis is important. Not everyone who is stable is going to be hooked up to the ACLS 150 mg of Amiodarone over 10 minute boiler plate treatment protocol. You might be giving electricity first. Or maybe Adenosine as a cure?

You should consider reading this article if you are

A huge EKG nerd

Fuzzy on the difference between “outflow tract” or “fascicular” ventricular tachycardias.

Under the impression that Adenosine is never used on VT or think that Adenosine can always be used on VT.

Wondering if there is a simplified (algorithmic) method of treating multiple subtypes of stable VT or if you need to be a cardiology fellow to figure this stuff out.